14S,21 R-DIHYDROXY DOCOSAHEXAENOIC ACID PROMOTES WOUND HEALING

Document Type

Presentation

Start Date

22-10-2010 10:45 AM

End Date

22-10-2010 12:00 PM

Description

Purpose-Based on the fact DHA is relatively abundant in wounded skin, and can be converted into bioactive lipid mediators, we hypothesized that wounding could induce this biosynthesis to generate a new lipid mediator, 14S,21-dihydroxy-docosahexaenoic acid (14S,21 R-diHDHA), which promote wound healing.

Methods-Biosynthesis of 14S,21 R-diHDHA was determined by LC-.UV-MS/MS analysis. 14S,21 R-diHDHA accelerating wound healing was assessed in splinted-excisional-wound healing models in C57BL/6J mice, as well as by C57BL/6J dermal microvascular endothelial cells (DMVECs) migration, vasculature formation and vascular endothelial growth factor (VEGF) expression in vitro. Phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) was valued by Western blot.

Results-Here we identified the formations of 14S,21 R-diHDHA in cutaneous wounds of C57BL/6J mice. Supplementation of exogenous 14S,21 R-diHDHA to wounds in animals rescued impaired healing and angiogenesis by accelerating wound re-epithelialization, granulation tissue formation, and vascularization. In the pivotal cellular processes of angiogenesis, 14S,21 RdiHDHA enhanced VEGF release, migration, and vasculature formation of DMVECs. Western blot revealed that 14S,21 R-diHDHA enhanceed phosphorylation of p38 MAPK in DMVECs.

Conclusion-Lipid mediator 14S,21 R-diHDHA promotes wound healing, and is a new lead for the development of better therapeutics treating impaired wound healing.

This document is currently not available here.

Share

COinS
 
Oct 22nd, 10:45 AM Oct 22nd, 12:00 PM

14S,21 R-DIHYDROXY DOCOSAHEXAENOIC ACID PROMOTES WOUND HEALING

Purpose-Based on the fact DHA is relatively abundant in wounded skin, and can be converted into bioactive lipid mediators, we hypothesized that wounding could induce this biosynthesis to generate a new lipid mediator, 14S,21-dihydroxy-docosahexaenoic acid (14S,21 R-diHDHA), which promote wound healing.

Methods-Biosynthesis of 14S,21 R-diHDHA was determined by LC-.UV-MS/MS analysis. 14S,21 R-diHDHA accelerating wound healing was assessed in splinted-excisional-wound healing models in C57BL/6J mice, as well as by C57BL/6J dermal microvascular endothelial cells (DMVECs) migration, vasculature formation and vascular endothelial growth factor (VEGF) expression in vitro. Phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) was valued by Western blot.

Results-Here we identified the formations of 14S,21 R-diHDHA in cutaneous wounds of C57BL/6J mice. Supplementation of exogenous 14S,21 R-diHDHA to wounds in animals rescued impaired healing and angiogenesis by accelerating wound re-epithelialization, granulation tissue formation, and vascularization. In the pivotal cellular processes of angiogenesis, 14S,21 RdiHDHA enhanced VEGF release, migration, and vasculature formation of DMVECs. Western blot revealed that 14S,21 R-diHDHA enhanceed phosphorylation of p38 MAPK in DMVECs.

Conclusion-Lipid mediator 14S,21 R-diHDHA promotes wound healing, and is a new lead for the development of better therapeutics treating impaired wound healing.